ArticleThe Journal of clinical investigation1999
Regulation of cardiac hypertrophy in vivo by the stress-activated protein kinases/c-Jun NH(2)-terminal kinases.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 176 citations in OpenAlex.
- Transforming growth factor-β and bone morphogenetic protein signaling pathways in pathological cardiac hypertrophy.Cell cycle (Georgetown, Tex.) · 2023Review
- The Role of PKC-MAPK Signalling Pathways in the Development of Hyperglycemia-Induced Cardiovascular Complications.International journal of molecular sciences · 2022Review
- Signaling cascades in the failing heart and emerging therapeutic strategies.Signal transduction and targeted therapy · 2022Review
- Molecules linked to Ras signaling as therapeutic targets in cardiac pathologies.Biological research · 2021Review
- Exosomally derived Y RNA fragment alleviates hypertrophic cardiomyopathy in transgenic mice.Molecular therapy. Nucleic acids · 2021Article
- JNK and cardiometabolic dysfunction.Bioscience reports · 2019Review
- Mixed lineage kinase-3 prevents cardiac dysfunction and structural remodeling with pressure overload.American journal of physiology. Heart and circulatory physiology · 2019Article
- The p21-activated kinase 1 (Pak1) signalling pathway in cardiac disease: from mechanistic study to therapeutic exploration.British journal of pharmacology · 2018Review
- Regulator of G protein signalling 14 attenuates cardiac remodelling through the MEK-ERK1/2 signalling pathway.Basic research in cardiology · 2016Article
- Dkk3 prevents familial dilated cardiomyopathy development through Wnt pathway.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- Electrical and mechanical stimulation of cardiac cells and tissue constructs.Advanced drug delivery reviews · 2016Review
- Dominant negative Ras attenuates pathological ventricular remodeling in pressure overload cardiac hypertrophy.Biochimica et biophysica acta · 2015Article
- Diet-induced obesity promotes altered remodeling and exacerbated cardiac hypertrophy following pressure overload.Physiological reports · 2015Article
- Tomoregulin-1 prevents cardiac hypertrophy after pressure overload in mice by inhibiting TAK1-JNK pathways.Disease models & mechanisms · 2015Article
- Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: therapeutic perspectives.Pharmacology & therapeutics · 2014Review
- MEK and the inhibitors: from bench to bedside.Journal of hematology & oncology · 2013Review
- Role of the Wnt-Frizzled system in cardiac pathophysiology: a rapidly developing, poorly understood area with enormous potential.The Journal of physiology · 2013Review
- The role of the paracrine/autocrine mediator endothelin-1 in regulation of cardiac contractility and growth.British journal of pharmacology · 2013Review
- JNK modulates FOXO3a for the expression of the mitochondrial death and mitophagy marker BNIP3 in pathological hypertrophy and in heart failure.Cell death & disease · 2012Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy often presages the development of heart failure. Numerous cytosolic signaling pathways have been implicated in the hypertrophic response in cardiomyocytes in culture, but their roles in the hypertrophic response to physiologically relevant stimuli in vivo is unclear. We previously reported that adenovirus-mediated gene transfer of SEK-1(KR), a dominant inhibitory mutant of the immediate upstream activator of the stress-activated protein kinases (SAPKs), abrogates the hypertrophic response of neonatal rat cardiomyocytes to endothelin-1 in culture. We now report that gene transfer of SEK-1(KR) to the adult rat heart blocks SAPK activation by pressure overload, demonstrating that the activity of cytosolic signaling pathways can be inhibited by gene transfer of loss-of-function mutants in vivo. Furthermore, gene transfer of SEK-1(KR) inhibited pressure overload-induced cardiac hypertrophy, as determined by echocardiography and several postmortem measures including left ventricular (LV) wall thickness, the ratio of LV weight to body weight, cardiomyocyte diameter, and inhibition of atrial natriuretic factor expression. Our data suggest that the SAPKs are critical regulators of cardiac hypertrophy in vivo, and therefore may serve as novel drug targets in the treatment of hypertrophy and heart failure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.